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March Flashcards

1
Q

Rheumatic fever develops due to infection of…

A

Streptococcus pyogenes (recent 2-6 weeks)

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2
Q

Immune response in rheumatic fever

A

B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated
there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry

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3
Q

What is M protein?

A

Virulence factor in cell wall of streptococcus pyogenes

Antibodies against M protein cross react with ryosin and smooth muscles of arteries

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4
Q

What gives rise to the clinical features in rheumatic fever?

A

Antibodies against M protein cross react with myosin and smooth musce of arteries

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5
Q

Name of the granulomatous bodies found in Rheumatic fever

A

Aschoff bodies

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6
Q

Diagnosis of Rheumatic fever

A

Recent streptococcus infection

2 major criteria or 1 major with 2 minor criteria

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7
Q

Major criteria for diagnossi of rheumatic fever

A

erythema marginatum
Sydenham’s chorea: this is often a late feature
polyarthritis
carditis and valvulitis (eg, pancarditis)
The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur)
subcutaneous nodules

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8
Q

Minore criteria for diagnosis of Rheumatic fever

A

raised ESR or CRP
pyrexia
arthralgia (not if arthritis a major criteria)
prolonged PR interval

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9
Q

Evidence of recent streptococcus infection

A

Antibodies raised
Positive throat swab
Positive rapid group A streptococcal antigen test

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10
Q

Management of rheumatic fever

A

antibiotics: oral penicillin V
anti-inflammatories: NSAIDs are first-line
treatment of any complications that develop e.g. heart failure

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11
Q

Patau syndrome is caused by which genetic abnormality

A

Trisomy 13

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12
Q

Which cardiac abnormality is most associated with Trisomy 13?

A

Ventricular septal defect

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13
Q

Which murmur may be heard with a ventricular septal defect?

A

Pansystolic murmur

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14
Q

AVSD is mostly associated with which syndrome?

A

Down’s Trisomy 21

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15
Q

Which condition is associated with coarctation of the aorta?

A

Marfans

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16
Q

What is Ebstein’s anomaly?

A

occurs when the tricuspid valve is displaced towards the apex of the right ventricle. It is a rare congenital heart disease and associated with added heart sounds on auscultation

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17
Q

Risk factor for Ebstein’s anomaly?

A

Maternal lithium used during pregnancy

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18
Q

Post natal presentations of VSD?

A 
failure to thrive
features of heart failure
hepatomegaly
tachypnoea
tachycardia
pallor
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19
Q

Management of moderate to severe VSD

A

nutritional support
medication for heart failure e.g. diuretics
surgical closure of the defect

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20
Q

Sign of aortic dissection on chest x-ray

A

Widened mediastinum

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21
Q

Type A aortic dissection occurs where?

A

Ascending aorta

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22
Q

Type B aortic dissection occurs where?

A

Descending aorta

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23
Q

Possible investigations of aortic dissection

A

Chest X -ray
CT Angiography of chest, abdomen, pelvis
Transoeosophageal echocardiography

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24
Q

Management of type A aortic dissection

A

Surgery - target systolic BP to 100-120

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25
Q

Management of Type B aortic dissection

A

Conservative
Bed rest
Reduce pressure with IV labetalol

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26
Q

Complications of aortic dissection

A

Complications of backward tear
aortic incompetence/regurgitation
MI: inferior pattern is often seen due to right coronary involvement

Complications of a forward tear
unequal arm pulses and BP
stroke
renal failure

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27
Q

What is electrical cardioversion synchronised to?

A

R wave

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28
Q

Name the subunits of troponin and what they bind to

A

troponin C: binds to calcium ions
troponin T: binds to tropomyosin, forming a troponin-tropomyosin complex
troponin I: binds to actin to hold the troponin-tropomyosin complex in place

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29
Q

Key suggestive finding of aortic dissection on CT

A

False lumen

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30
Q

Blurring of the posterior wall of the descending aorta on CT is a sign of ???

A

retroperitoneal, contained rupture of an aortic aneurysm. This may present with hypovolaemic shock (hypotension, tachycardia, tachypnoea) and collapse.

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31
Q

Classic presentation of rupture aortic aneurysm

A

Shock
Abdominal pain radiating to the back
Pulsatile mass

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32
Q

How is recurrent DVT in cancer patients who are adequately anticoagulated managed?

A

‘Consider inferior vena caval filters for patients with recurrent proximal DVT or PE despite adequate anticoagulation treatment only after considering alternative treatments such as:
increasing target INR to 3–4 for long term high-intensity oral anticoagulant therapy or
switching treatment to LMWH.’

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33
Q

Most common cause of sudden cardiac death in the young?

A

HOCM - Hypertrophic Obstructive Cardiomyopathy

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34
Q

What is Hypertrophic Obstructive Cardiomyopathy?

A

autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins

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35
Q

Pattern of inheritance of HOCM

A

Autosomal dominant

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36
Q

Genetic defect in HOCM

A

mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C

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37
Q

Describe the cardiac dysfunction seen in HOCM and effect on cardiac output

A

results in predominantly diastolic dysfunction

left ventricle hypertrophy → decreased compliance → decreased cardiac output

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38
Q

Features of HOCM

A

often asymptomatic
exertional dyspnoea
angina
syncope
typically following exercise
due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
jerky pulse, large ‘a’ waves, double apex beat
ejection systolic murmur
increases with Valsalva manoeuvre and decreases on squatting
hypertrophic cardiomyopathy may impair mitral valve closure, thus causing regurgitation

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39
Q

When is syncope likely to occur in someone with HOCM?

A

Following exercise

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40
Q

What type of murumur is present in HOCM?

A

Ejection systolic murmur
Decreases on squatting
Increases with valsalva manouevre

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41
Q

Name two associations with HOCM

A

Friedreich’s ataxia

Wolff-Parkinson White

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42
Q

ECHO findings in HOCM

A

MR SAM ASH
Mitral reurg
Systolic anterior motion of anterior mitral valve leaflet
Assymetric hypertrophy

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43
Q

ECG findings in HOCM

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen

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44
Q

What is murphy’s sign?

A

Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive

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45
Q

LFT results in cholecystitis

A

raised ALP and liver transaminases. The ALP level result in cholestatic diseases however, is usually raised to a much greater extent than liver transaminases.

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46
Q

Causes of gynaecomastia

A 
Obesity
Testicular cancer
Cannabis
Alcohol
Klinefelter syndrome
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47
Q

Why does gynaecomastia occur in testicular cancer?

A

Increased oestrogen:androgen ratio

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48
Q

AFP is a tumour marker for which cancers?

A

Testiuclar

Hepatocellular carcinoma

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49
Q

Mechanism of dipyridamole

A

non-specific phosphodiesterase inhibitor and decreases cellular uptake of adenosine
elevating platelet cAMP levels which in turn inhibits platelet aggregation and thrombus formation
Inhibits thromboxane synthase

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50
Q

Indication of dipyridamole

A

an antiplatelet mainly used after an ischaemic stroke, transient ischaemic attack or prosthetic valve replacement

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51
Q

action of a direct oral anticoagulant (DOAC), an example being dabigatran.

A

Factor Xa antagonist

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52
Q

mechanism of antiplatelet agents such as clopidogrel and ticagrelor.

A

P2Y12 receptor antagonists

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53
Q

Hyperacute transplant rejection is caused by

A

pre-existing antibodies against ABO or HLA antigens

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54
Q

Branches of the external carotid

A

eight branches
3 from its anterior surface ; thyroid, lingual and facial. The pharyngeal artery is a medial branch.
The posterior auricular and occipital are posterior branches.

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55
Q

Why does nephrotic syndrome have increased risk of arterial and venous thrombosis?

A

loss of antithrombin III via the kidneys

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56
Q

Complications of nephrotic syndrome

A

increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine

deep vein thrombosis, pulmonary embolism
renal vein thrombosis, resulting in a sudden deterioration in renal function

hyperlipidaemia
increasing risk of acute coronary syndrome, stroke etc
chronic kidney disease
increased risk of infection due to urinary immunoglobulin loss
hypocalcaemia (vitamin D and binding protein lost in urine)

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57
Q

Presenting features of Wernicke encephalopathy

A

ataxia, ophthalmoplegia and/or encephalopathy

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58
Q

Features of Korsakoff’s syndrome

A

chronic neurological deterioration that is characterised by deficits in anterograde and retrograde memory which leads to confabulation

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59
Q

Wernicke-korsakoff syndrome occurs due to which deficiency seen in which groups of patients

A

Thiamine deficiency

Alcoholic

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60
Q

Symptoms of alcohol withdrawal

A

disorientation, confusion, sweating, tremor, agitation, and anxiety.

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61
Q

Wernicke’s encephalopathy untreated leads to which condition?

A

Korsakoff’s syndrome

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62
Q

What is reaction formation?

A

transforming an unacceptable feeling or impulse into its extreme opposite. Instigating a physical fight with his boyfriend’s other partner would be an example of reaction formation.

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63
Q

What is sublimation?

A

Replacing an unacceptable wish with a course of action that is similar to the wish but does not conflict with one’s value system
a mature ego defence mechanism whereby one channels unacceptable thoughts, feelings or impulses into socially acceptable alternatives.

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64
Q

how does gentamicin cause AKI?

A

Renal cell apoptosis

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65
Q

Which drug used in triple therapy for infective endocarditis can cause AKI?

A

Gentamicin

Triple therapy - gentamicin, vancomycin, amoxicillin

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66
Q

How does penicillin cause AKI?

A

Acute interstitial nephritis

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67
Q

Genetic mutations in nephrogenic diabetes

A

the more common form affects the vasopression (ADH) receptor

the less common form results from a mutation in the gene that encodes the aquaporin 2 channel

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68
Q

The vasopressin receptor mutation in nephrogenic diabetes is which type of mutation

A

X linked

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69
Q

Mutation in the genes endoign the aquaporin 2 channel seen in nephrogenic diabetes is inherited how?

A

Autosomal recessive

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70
Q

2 aims of treatment in management of hyperkalaemia

A

Stabilise cardiac membrane - calcium gluconate
Short-term shift in potassium from extracellular to intracellular fluid compartment - insulin/dextrose infusion, nebulised salbutamol, loop diuretics, calcium resonium, dialysis

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71
Q

What type of drug is nicorandil and mechanism of action?

A

vasodilatory drug used to treat angina. It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

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72
Q

Adverse effects of nicorandil

A

Headache
Flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration

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73
Q

Contraindications of nicorandil

A

Left ventricular failure

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74
Q

Drugs that must be stopped in AKI

A

non-steroidal anti-inflammatory drugs
aminoglycoside antibiotics (e.g. gentamicin)
angiotensin-converting enzyme inhibitors (e.g. ramipril), angiotensin II receptor antagonists (e.g. losartan
diuretics.

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75
Q

Terlipressin is used to treat

A

vasopressin-analogue used in the treatment of haemorrhage from oesophageal varices

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76
Q

Desmopressin is used in treatment of which condition

A

Central diabetes insipidus

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77
Q

Goserelin is used to treat which condition

A

Prostate cancer

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78
Q

Indapamide is used to treat which conditions

A

Thiazide like diuretic - heart failure and hypertension

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79
Q

Carbimazole is used to treat which condition

A

Hyperthyroidsim

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80
Q

2 forms of diabetes insipidus

A

decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI)
or an insensitivity to antidiuretic hormone (nephrogenic DI).

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81
Q

Causes of cranial diabetes insipidus

A 
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
histiocytosis X
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome)
haemochromatosis
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82
Q

Causes of nephrogenic Diabetes Insipidus

A

genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes: hypercalcaemia, hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

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83
Q

Features of diabetes insipidus

A

Polyuria

Polydipsia

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84
Q

Investigation of diabetes insipidus

A

high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test

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85
Q

What type of condition is familial hypercholesterolaemia?

A

Autosomal dominant

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86
Q

Effect of alcohol on ACE-i

A

Alcohol compounds the antihypertensive effects of ACE inhibitors

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87
Q

Trend in bloods in refeeding syndrome

A

A large release of insulin in refeeding syndrome causes a rapid shift of K+, Mg2+ and PO4- into cells, causing hypokalaemia, hypophosphataemia and hypomagnesemia

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88
Q

Mode of inheritance of Alport’s Syndrome

A

X-linked dominant

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89
Q

What is the genetic defect in Alport’s syndrome?

A

type IV collagen resulting in an abnormal glomerular-basement membrane (GBM).

90
Q

When does Alport’s syndrome usually present?

A

In childhood

91
Q

Features of Alport’s syndrome

A

microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy

92
Q

How is Alport’s syndrome diagnosed?

A

Renal biopsy#

Molecular genetic testing

93
Q

Where in the nephron does the maority of glucose reabsoprtion occur?

A

Proximal convoluted tubule

94
Q

What is the mechanism of empagliflozin?

A

inhibitor of the SGLT-2 receptor and prevents glucose reabsorption in the nephron.

95
Q

Complications of diabetic nephropathy are due to…

A

Non-enzymatic glycosylation (NEG) of the vascular membrane occurs in both large and medium vessels leading to atherosclerosis. NEG of small vessels results in hyaline arteriosclerosis, which in the renal efferent arteriole results in sclerosis of the glomerulus leading to nephropathy.

96
Q

What occurs in the kidneys in rhabdomyolysis following a fall?

A

damaged muscles release myoglobin which is nephrotoxic and causes renal ischaemia, the pathology of acute tubular necrosis

97
Q

Treatment for rhabdomyolysis

A

IV fluids

98
Q

Histological findings for membranous glomerulonephritis

A

basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2

99
Q

Features of hypocalcaemia

A

perioral paraesthesia, cramps, tetany and convulsions

100
Q

Vitamin B1 is also known as

A

Thiamine

101
Q

How do nitrates induce smooth muscle relaxation?

A

Nitric oxide activates smooth muscle soluble guanylyl cyclase (GC) to form cGMP. Increased intracellular cGMP inhibits calcium entry into the cell, thereby decreasing intracellular calcium concentrations and causing smooth muscle relaxation (click here for details).

102
Q

Second line therapy when patient unable to tolerate statin (leg cramps)

A

The second line therapy for patients who are unable to tolerate the side effects of statins is ezetimibe

103
Q

Which hormone is insufficient in cranial DI?

A

Antidiuretic hormone

Kidneys cannot concentrate urine even when hypovolaemic

104
Q

Symptoms of cranial DI

A

Polyuria
Pale urine
Chronic thirst

105
Q

Causes of cranial DI

A

Head trauma
Localised infection
Post-radiotherapy

106
Q

What investigation can be used to diagnose cranial DI

A

Water deprivation test

107
Q

Result of water deprivation test after fluid deprivation in cranial DI

A

Low urine osmolality

108
Q

Result of water deprivation test after desmopressin in cranial DI

A

High urine osmolality

109
Q

Affect of thyroid disease on muscles

A

Myopathy

110
Q

Sign of myopathy in muscle biopsy

A

Cells of all different sizes - necrosis and regenration : Checkerboard pattern

111
Q

Causes of thyrotoxicosis

A

Graves’ disease
toxic nodular goitre
acute phase of subacute (de Quervain’s) thyroiditis
acute phase of post-partum thyroiditis
acute phase of Hashimoto’s thyroiditis (later results in hypothyroidism)
amiodarone therapy

112
Q

Investigation of thyrotoxicosis

A

TSH down, T4 and T3 up
thyroid autoantibodies
other investigations are not routinely done but includes isotope scanning

113
Q

Features in Grave’s disease but not in other causes of thyrotoxicosis

A 
eye signs (30% of patients)
exophthalmos
ophthalmoplegia
pretibial myxoedema
thyroid acropachy, a triad of:
digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formation
114
Q

Which hormone acts on satiety centres in hypothalamus to decrease appetite?

A

Leptin

115
Q

Where is leptin produced?

A

Adipose tissue

116
Q

Obesity results in what level of leptin?

A

Higher levels - more adipose

117
Q

Leptin stimulates the release of which hormones

A

stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH). Low levels of leptin stimulates the release of neuropeptide Y (NPY)

118
Q

Where is the hormone ghrelin produced?

A

P/D1 cells lining the fundus of the stomach and epsilon cells of the pancreas

119
Q

What effect does ghrelin have on hunger and how do the levels change with meals?

A

Increases hunger
High before meal
Low after meal

120
Q

How does stiptagliptin reduce blood glucose levels?

A

It works by inhibiting an enzyme responsible for breaking down incretin, and so leads to increased incretin levels. Increased incretin levels then work to decrease blood glucose levels.

121
Q

Which class of diabetic drugs is stiptagliptin?

A

DPP4 inhibitor

122
Q

Dapagliflozin is which type of diabetic drug?

A

SGLT2 inhibitor

123
Q

How do SGLT2 inhibitors reduce blood glucose?

A

Reduce reabsoprtion of glucose in the kidneys

124
Q

How does metformin reduce blood glucose levels?

A

Increases peripheral uptake of insulin

125
Q

Most common cause of hypothyroidism

A

Iodine deficiency

ASK ABOUT DIET

126
Q

What is Hashimoto’s thyroiditis?

A

autoimmune condition resulting in an inflammation, thus goitre formation, and reduction in thyroid function. The thyroid gland is attacked by a variety of cell and antibody-mediated immune processes such as antibodies to thyroglobulin or thyroid peroxidase resulting in low amounts of T4 and T3 are being produced and released

127
Q

What is the association with Hashimoto’s thyroiditis?

A

Other autoimmune conditions eg diabetes, pernicious anaemia

128
Q

How does secondary hypothyroidism occur?

A

Pituitary failure

129
Q

Associations with secondary hypothyroidism

A

Down’s syndrome
Turner’s syndrome
coeliac disease

130
Q

What tumour marker is monitored for medullary thyroid cancer recurrence?

A

Calcitonin

131
Q

What other electrolyte imbalance can make hypocalcaemia resistant to treatment?

A

Hypomagnesemia

132
Q

What is metabolic syndrome?

A

A clustering of cardiovascular risk factors

133
Q

Diagnostic criteria for metabolic syndrome

A
  • Increased waist circumference (dependent on ethnicity) or a BMI >30
  • Dyslipidaemia with raised triglycerides >150 mg/dL or reduced HDL-cholesterol
  • Hypertension
  • Impaired glucose tolerance
134
Q

Features of hyperparathyroidism

A

Features - ‘bones, stones, abdominal groans and psychic moans’
polydipsia, polyuria
peptic ulceration/constipation/pancreatitis
bone pain/fracture
renal stones
depression
hypertension

135
Q

Causes of primary hyperparathyroidism

A

80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

136
Q

Associations with primary hyperparathyroidism

A

Hypertension

MEN I and II

137
Q

Investigations for primary hyperparathyroidism

A

raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal
technetium-MIBI subtraction scan
pepperpot skull is a characteristic X-ray finding of hyperparathyroidism

138
Q

Treatment of primary hyperparathyroidism

A

the definitive management is total parathyroidectomy
conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
calcimimetic agents such as cinacalcet are sometimes used in patients who are unsuitable for surgery

139
Q

Features of Addison’s disease

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

140
Q

What is not produced in Addison’s?

A

Aldosterone, cortisol

141
Q

What is the function of aldosterone?

A

Sodium reabsorption

Potassium excretion

142
Q

How do sulphonylureas lower blood sugar?

A

mimicking the role of ATP on potassium-ATP channels block these channels causing membrane depolarisation and thus opening of voltage-gated calcium channels.

stimulation of insulin release.

143
Q

Main side effect of sulfonylureas

A

Hypoglycaemia

144
Q

Major complication of sulfonylureas

A

Neuroglycopenia

145
Q

Signs of neuroglycopenia and how is it treated?

A

Confusion, coma
Oral glucose
Intramuscular glucagon
IV glucose

146
Q

What antibodies are developed in grave’s disease

A

IgG to TSH receptors on thyroid gland

147
Q

Why is liver disease associated with gynaecomastia?

A

Impaired oestrogen metabolism

148
Q

Which cells secrete growth hormone?

A

Somatotroph cells in anterior pituitary

149
Q

Features of excess growth hormone

A

thickened skin, enlarged hands and feet, a prominent jaw, carpal tunnel syndrome, tiredness, muscle weakness and hypertension.

150
Q

Excess growth hormone can increase the risk of which condition

A

Type II diabetes

151
Q

Why does excess growth hormone increase the risk of type 2 diabetes?

A

Glucose moves from muscle into blood

Pancreas secretes more insulin in response to lower blood glucose

152
Q

What can increase growth hormone secretion?

A

GHRH
Fasting
Sleeping
Exercise

153
Q

What decreases growth hormone secretion?

A

Glucose

Somatostatin

154
Q

What results from insufficient growth hormone levels?

A

Short stature

155
Q

Where is ADH secreted?

A

Posterior pituitary

156
Q

Function of ADH

A

Water reabsorption - inserts Aquaporin 2 channels in collecting ducts of kidneys

157
Q

What condition arises from ADH deficiency?

A

Diabetes insipidus

158
Q

What increases ADH secretion?

A

Decrease in blood pressure
Volume dcrease
ECF osmolality increase
Angiotensin II

159
Q

What decreases ADH secretion?

A

Volume increase
Temperature decrease
ECF osmolality decrease

160
Q

How is cranial DI treated?

A

Desmopressin -ADH analog

161
Q

Difference in general symptoms of hypothyroidism and thyrotoxicosis?

A

Weight gain, cold intolerance, lethargy - hypothyroidism

Weight loss, heat intolerance, manic/restlessness - thyrotoxicosis

162
Q

Which anti-diabetic drugs are weight-neutral?

A

Gliptins - DPP4 inhibitors

163
Q

Thiazolidinediones (e.g. pioglitazone) activate the peroxisome proliferator-activated receptor gamma (PPAR gamma). Which condition are they contraindicated in?

A

Heart failure

164
Q

Side effect of SGLT2 inhibitors

A

Promote renal glucose ecretion - glycosuria leading to increased UTIs

165
Q

Risk factors of high level of steroid use

A 
Hyperglycemia
High blood pressure
Obesity (above the waste and not limbs)
Wasting of skeletal muscles
Poor wound healing
Mood swings and depression
166
Q

What is Bartter’s Syndrome?

A

An inherited cause of severe hypokalemia due to mutation in NaK2CL cotransporter in loop of henle

167
Q

Features of Bartter’s Syndrome

A 
Presents in childhood - failure to thrive
Polyuria, polydipsia
Hypokalemia
Normotension
Weakness
168
Q

What diuretic response can Bartter’s syndrome be likened to ?

A

Taking large doses of furosemide - inhibits same cotransporter NKCC2

169
Q

Cells of anterior pituitary gland

A 
50% somatotrophs. 
Roughly 15% of the cells are lactotrophs, 
15% corticotrophs, 
10% gonadotrophs and 
5% thyrotrophs. 
The remaining 5% are supporting cells.
170
Q

What is Waterhouse Friederichsen syndrome?

A

Waterhouse-Friderichsen syndrome is adrenal gland failure due to bleeding into the adrenal gland.

171
Q

What is the most common bacterial cause of Waterhouse Friederichsen syndrome?

A

Neisseria meningitidis

172
Q

Clinical feautres of Klinefelter’s syndrome

A

poor coordination, muscle weakness, reading difficulties, gynaecomastia, secondary sexual characteristic development delay, taller than average, rounded body, and microorchidism.

173
Q

Karyotype for Klinefelter’s syndrome

A

47 XXY

174
Q

Mnemonic for hypercalcaemia - CHIMPANZEES

A 
C alcium supplementation
H yperparathyroidism
I atrogentic (Drugs: Thiazides)
M ilk Alkali syndrome
P aget disease of the bone
A cromegaly and Addison's Disease
N eoplasia
Z olinger-Ellison Syndrome (MEN Type I)
E xcessive Vitamin D
E xcessive Vitamin A
S arcoidosis
175
Q

Increased secretion of insulin

A 
Glucose
Amino acid
Vagal cholinergic
Secretin/Gastrin/CCK
Fatty acids
Beta adrenergic drugs
176
Q

What drugs inhibit insulin release?

A

Beta blockers

177
Q

Twitching of the facial muscles on tapping is known as which signs and why does it occur?

A

Chvostek’s sign is seen in hypocalcaemia due to increased irritability of the peripheral nerves

178
Q

Why does hyperthyroidism cause weight loss?

A

Thyroid hormones increase basal metabolic rate - by affecting protein synthesis
In growth - increase sensitivity to catecholamines

179
Q

Explain thyroid hormone effect on catabolism and subsequent lipolysis

A

Thyroid hormones act on the membrane stimulating the sodium-potassium pump thereby increasing the uptake and catabolism of glucose and amino acids. This results in a calorigenesis while also acting on the mitochondria for ATP formation for the pump. the catabolic effects on fat mean they are lipolytic and thus increase cholesterol breakdown and LDL receptors.

180
Q

Other metabolic effects of thyroid hormones

A
  • Increased gut motility and intestinal glucose absorption
  • Increase hepatic glycogenolysis
  • Potentiation of insulin’s effects on liver and muscle for glucose uptake
  • Breaking down of insulin to prevent glucose storage
  • Potentiation of the glycogenolysis effects of Adrenaline
181
Q

Cardiac and respiratory effects of thyroid hormones

A

increasing oxygen consumption, they also act to increase erythropoiesis for more oxygen transport, increase cardiac contractility and maintain the hypoxic and hypercapnic drive in the respiratory centre.

182
Q

First-line treatment of acromegaly

A

Trans-sphenoidal surgery

183
Q

Indication for medication to treat acromegaly

A

Surgery unsuccessful or pituitary tumour inoperable

184
Q

Medications used to treat acromegaly

A

Somatostatin analogue
Pigvesomant - s/c
Dopamine agonists

185
Q

Which type of drug is octreotide and what is its mechanism?

A

Somatostatin analogue

Directly inhibits growth hormone release

186
Q

Features of cardiac tamponade presentation

A

Can present in shock

muffled heart sounds, elevated JVP, and dyspnoea

187
Q

Where is prolactin secreted from>

A

Anterior pituitary

188
Q

What inhibits prolactin release?

A

Dopamine

189
Q

What increases prolactin secretion?

A 
Pregnancy
Thyrotropin releasing hormone
Oestrogen
Breast feeding
Sleep 
Stress
DRugs - metaclopramide, antipsychotics
190
Q

Side effect of carbimazole

A

Bone marrow suppression - neutropenia, agranulocytosis

Sore throat

191
Q

Which symptom if arises suggests stopping treatment with carbimazole?

A

Sore throat

192
Q

Which condition is treated using carbimazole?

A

Grave’s disease

193
Q

consequences of metabolic syndrome - diabetes and hypertension present in patient with chest pain as case example

A
  • Strokes
  • Non-insulin dependant diabetes
  • Cardiovascular disease
  • Cancers - including breast, colon and endometrial
  • Polycystic ovarian syndrome
  • Obstructive sleep apnea
  • Fatty liver
  • Gall stones
  • Mental health problems
194
Q

What is the mode of inheritance of Haemochromatosis

A

Autosomal recessive

195
Q

What type of disorder is haemochromatosis?

A

Iron absorption resulting in accumulation

196
Q

Investigation for haemochromatosis?

A

Transferrin saturation

197
Q

Diagnostic test for haemochromatosis

A

molecular genetic testing for the C282Y and H63D mutations

liver biopsy: Perl’s stain

198
Q

Iron study profile for haemochromatosis

A

transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC

199
Q

Management of haemochromatosis

A

Venesection

desferrioxamine as second line - long-term iron chelation

200
Q

Example presentation of haemochromatosis

A

A 45-year-old man has chronic liver disease. He presents with chronic progressive pain in his metacarpophalangeal and proximal interphalangeal joints. He does not complain of joint stiffness but mentions that he cannot get an erection. His sister developed a similar set of problems when she was 55-years-old.

On examination, he has grey skin, hepatomegaly, and swollen joints in his hands.

201
Q

Main risk factor for developing hepatocellular carcinoma

A

Cirrhosis

202
Q

Cirrhosis can occur secondary to?

A

hepatitis B & C,
alcohol,
haemochromatosis
and primary biliary cirrhosis.

203
Q

Risk factor for hepatocellular carcinoma

A 
alpha-1 antitrypsin deficiency
hereditary tyrosinosis
glycogen storage disease
aflatoxin
drugs: oral contraceptive pill, anabolic steroids
porphyria cutanea tarda
male sex
diabetes mellitus, metabolic syndrome
204
Q

Signs of hepatocellular carcinoma

A 
Features of cirrhosis
jaundice
ascites
RUQ pain
hepatomegaly
pruritus
splenomegaly
Raised AFP
205
Q

Screening of hepatocellular carcinoma

A

Ultrasound

AFP

206
Q

Management of hepatocellular carcinoma

A 
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
207
Q

Why is metaclopramide contraindicated in bowel obstruction?

A

It is a pro kinetic antiemetic - can cause bowel perforation

208
Q

Acute treatment of variceal haemorrhage

A

ABC
Correct clotting - FFP, vitamin K
Vasoactive agents - terlipressin, octreotide
Prophylactic antibiotics - quinolones
Endoscopic variceal band ligation
Sengstaken Blakemore tube if bleeding persists
Transjugular Intrahepatic Portosystemic Shunt (tips)

209
Q

Prophylaxis of variceal haemorrhage

A

Propanolol

Endoscopic variceal band ligation

210
Q

How is Ulcerative Colitis classed by severity?

A

Mild - less than 4 stools a day, small amount of blood
Moderate - 4 to 6 stools a day, varying blood, no systemic upset
Severe - more than 6 bloody stools a day, systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

211
Q

Omeprazole and other PPIs are associated with which side effect?

A

Hyponatraemia

212
Q

Features of Budd Chiari Syndrome

A

abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly

213
Q

Causes of budd chiari syndrome

A

Polycythaemia vera
Thrombophilia
Pregnancy
COCP

214
Q

Invesitgation for Budd Chiari Syndrome (hepatic vein thrombosis)

A

Ulstrasound doppler

215
Q

Management of ascites

A 
Sodium and fluid restriction
Aldosterone antagonists - spironolactone
- can add loop diuretic
Drainage if tesne
Prophylactic antibiotics
TIPS
216
Q

Acetazolimide is which type of drug and used for treatment of which condition

A

Carbonic anhydrase inhibitor

Glaucoma

217
Q

Triad of mesenteric bowel ischaemia

A

CVD, high lactate and soft but tender abdomen

218
Q

Predisposing factors to bowel ischaemia

A

Age
AF
Endocarditis, malignancy - causes of emboli
Cardiovascular risk factors - smoking, diabetes, hypertension
Cocaine

219
Q

Common features of bowel ischaemia

A

abdominal pain - in acute mesenteric ischaemia this is often of sudden onset, severe and out-of-keeping with physical exam findings
rectal bleeding
diarrhoea
fever
bloods typically show an elevated white blood cell count associated with a lactic acidosis

220
Q

Diagnostic investigation of mesenteric bowel ischaemia

A

CT

221
Q

Most common organisms of liver abscess

A

Children - Staph aureus

Adult - E coli

222
Q

Managmeent of liver abscess

A

Drainage and antibiotics
Amoxicilllin, metronidazole and ciprofloxacin
Clindamycin if penicillin allergic

Finals random (5 decks)

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